Journal
BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY
Volume 29, Issue 2, Pages 233-244Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.bpg.2015.02.002
Keywords
Cholangiocarcinoma; Molecular pathogenesis; Genetic alteration; Chromatin
Categories
Funding
- Singapore National Medical Research Council [NMRC/STAR/0006/2009]
- Bronsveld Foundation [25560830]
- Lee Foundation [26960760]
- Tanoto Foundation [26961350]
- Singapore National Cancer Centre Research Fund [25560850]
- Duke-NUS Graduate Medical School [R-913-200-070-263]
- Cancer Science Institute, Singapore [R-713-006-011-271]
- Verdant Foundation, Hong Kong [N-918-041-003-001]
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Cholangiocarcinoma (CCA) is a malignant tumour of bile duct epithelial cells with dismal prognosis and rising incidence. Chronic inflammation resulting from liver fluke infection, hepatitis and other inflammatory bowel diseases is a major contributing factor to cholangiocarcinogenesis, likely through accumulation of serial genetic and epigenetic alterations resulting in aberration of oncogenes and tumour suppressors. Recent studies making use of advances in high-throughput genomics have revealed the genetic landscape of CCA, greatly increasing our understanding of its underlying biology. A series of highly recurrent mutations in genes such as TP53, KRAS, SMAD4, BRAF, MLL3, AR1D1A, PBRM1 and BAP1, which are known to be involved in cell cycle control, cell signalling pathways and chromatin dynamics, have led to investigations of their roles, through molecular to mouse modelling studies, in cholangiocarcinogenesis. This review focuses on the landscape genetic alterations in CCA and its functional relevance to the formation and progression of CCA. (C) 2015 Elsevier Ltd. All rights reserved.
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